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The appearance of the omicron variant of COVID-19 sparked a new wave of pandemic panic around the world, with many countries closing their borders and imposing new lockdowns. But the more clearly the less dangerous the new pathogen strain becomes, the more the scientific knowledge confirms that other deadly viruses have mutated into everyday diseases.

Omicron has been on everyone’s lips around the world in recent months, as the new COVID-19 variant spread rapidly from southern Africa to all other inhabited continents.

However, some governments are now rethinking their initial reactions to the latest variant, as doctors’ initial observations from South Africa confirm that the symptoms are “very mild” even though it is far more contagious.

In Gauteng, the South African province at the center of the outbreak, it quickly ousted the previously dominant delta variant. The UK Health Authority estimated it to have reached 90 percent dominance in the UK by December 26th.

In a speech about the Omicron variant earlier this month, Russian President Vladimir Putin stated that “some experts even refer to it as a ‘live vaccination'”.

On Monday the British government announced that it would not tighten restrictions any further so that New Years Eve celebrations in England can continue.

But long before Omikron appeared in Botswana, virologists had predicted that the virus – which killed around 5 million people worldwide – would eventually evolve into a near-harmless form, which, ironically, would give it a selective advantage over previous variants.

A novel H1N1 strain of influenza caused the post-World War I pandemic of 1918, which killed 25-50 million people worldwide. By 1920, however, it had mutated into a much milder form that could no longer be distinguished from other seasonal flu viruses. Will COVID-19 follow the same path?

Evil is not always stronger

The basic concept is simple: in order to thrive and continue its genetic line, a virus must spread from organism to organism. A virus that kills its host quickly has fewer opportunities to infect new hosts.

In contrast to bacteria and amoeba pathogens, viruses cannot live and multiply freely in nature. For a long time, science has been divided as to whether viruses are real living organisms because they do not have their own replication mechanisms. Instead, they use the biochemical machinery of the cells they infect to make copies of their genetic material and the building blocks of the protein envelope that surrounds it.

I believe viruses tend to become less pathogenic, “Burtram Fielding, corona aviologist at the University of the Western Cape in South Africa, told Knowable magazine last year. “The ultimate goal of a pathogen is to multiply in order to produce more of itself. A pathogen that kills the host too quickly does not have enough time to multiply.

Precisely the actions governments and health authorities have taken in response to the pandemic – including quarantine and contact tracing – could create an artificially selective disadvantage for serious diseases by hindering their spread in ways that the common cold does not is.

One of the main characteristics of COVID-19 is that the infected patient becomes contagious before showing symptoms. In contrast to viruses such as measles or smallpox, which the World Health Organization declared eradicated in 1980 after almost 200 years of immunization, those who are vaccinated can still transmit the disease if they do not get sick due to their immunity.

Variants of COVID-19 with higher virulence – the ability to make sick or kill – will be easier to spot and patients will be isolated more quickly, say those who have experienced previous pandemics.

Immunologist Mark Cameron of Case Western Reserve University in Cleveland was on staff at a Toronto hospital at the height of the SARS pandemic in 2003. “People who contracted SARS got sick very quickly and were easily identified, tracked and quarantined – and their contacts were also easily identified and quarantined,” he told Knowable.

Mutation to the point of extinction

Another factor that helps neuter new pandemic viruses is exactly what makes them arise in the first place – often by jumping from one species to another, as is suspected in the case of COVID-19 – their ability to grow in a short period of time mutate and evolve.

Coronavirus is one of many viruses whose genetic information is carried on a single strand of RNA, the long-chain molecule that translates the DNA of living cells into the proteins they code for. This class of viruses, which use the enzyme RNA-dependent RNA polymerase from host cells to copy their gene strand, are known for their very high mutation rates.

“The evolution of RNA viruses is so rapid that it can often be observed in real time,” stated Edward Holmes, then from Pennsylvania State University, in a 2009 paper, on the order of one point change in code per replication.

Holmes was referring to previous research on vesicular stomatitis virus (VSV), another RNA-based pathogen. They found that around 40 percent of the mutations cause this line of the pathogen to die out. Another 30% were generally harmful to the survival of the pathogen, and more than 25% had only a neutral effect. Only five percent of the mutations were actually beneficial for the virus and improved its chances of survival.

The paper also discussed how a high mutation rate can provide a selection advantage by producing beneficial new traits more quickly, while too high a rate can be counterproductive in preventing the good mutations from stabilizing in the population.

The fittest genotype can be wiped out by the appearance of a harmful random mutation, an event known as a “failure catastrophe.” Another phenomenon is the “extinction threshold” being exceeded in a population in which bad mutations accumulate faster than natural selection can eradicate them.

The spread of the Delta variant from India in mid-2021, as vaccination campaigns were just making headway in many countries, sparked concerns about the bacterium’s alleged ability to “break” immunity and its alleged high virulence.

But something strange happened in Japan. After the number of daily cases peaked at over 26,000 in late summer, Delta mysteriously began to wane. By November of this year, only about 200 cases were detected each day.

A team of researchers from the National Institute of Genetics and Niigata University, led by Professor Ituro Inoue, suggested that the virus had mutated into “self-destruction”. Inoue’s theory is that the virus had acquired too many mutations in its gene for an error-correcting protein called nsp14.

“We were literally shocked to see the results,” Inoue told the Japan Times. “The delta variant in Japan was highly transferable and kept other variants out. But as the mutations piled up, we believe it eventually turned into a buggy virus and was no longer able to make copies of itself. “

“Given that the number of cases has not increased, we believe that the virus headed for natural extinction at some point during these mutations,” concluded the professor.

Inoue believes SARS suffered the same fate in 2004 – but that cannot be proven as the virus is now gone.

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